(+)-Catechin, an ingredient of green tea, protects murine microglia from oxidative stress-induced DNA damage and cell cycle arrest.

Extracts of Chinese herbs have been demonstrated to inhibit oxidative stress in vitro. In this study, we investigated the mechanism of (+)-catechin, isolated from green tea, which preserved murine microglia N9 cells from an oxidative agent tert-butylhydroperoxide (tBHP)-induced cell death. (+)-Catechin augmented the cell survival ratio after exposure to tBHP. Protective action of this drug was more efficacious than that of N-acetylcysteine, which is a putative antioxidant. DNA damage, detected by the Comet assay, was diminished with treatment of the drug. Results of flow cytometric analysis showed that the amount of intracellular *OH was decreased, and the cell cycle arrest was reversed by down-regulation of p53 phosphorylation after treatment with (+)-catechin. The reduced p53 activity followed the impairment of NF-kappaB translocation to the nuclear region. Then the phosphorylation of extracellular signal regulated protein kinase, a cell survival facilitative signal, was upregulated at the later stage. Taken together, (+)-catechin inhibited tBHP-induced translocation of NF-kappaB to improve cellular survival.